The metabolic response to food intake is regulated by gastro-intestinal and other peptide hormones and energy intermediate metabolites. However, intake must be regulated to maintain certain plasma metabolites (e.g. glucose) within a safe physiological range. This complex balance is co-ordinated by the brain, and uses a variety of neural, hormonal and metabolite signals to monitor energy status. Some signals are peptide hormones (referred to here as “gut hormones”) released from various parts of the body in response to a perceived energy status. These include those secreted by gastrointestinal endocrine cells such as glucose-dependent insulinotropic peptide (GIP). Such peptide hormones have short half-lives enabling a dynamic response to changing conditions. This allows their levels to be determined, analysed and correlated to food intake across a time period.
After a meal, gut hormones are secreted into the circulation in order to stimulate insulin secretion. GIP is one of these “incretin” hormones and blood levels are elevated in obesity and diabetes. GIP exerts various peripheral effects on adipose tissue and lipid metabolism, leading to increased lipid deposition in the post prandial state. GIP stimulates pro-inflammatory gene expression in adipose tissue and impairs insulin sensitivity. Blockade of GIP signalling has been shown to cause preferential oxidation of fat and to clear triacylglycerol deposits from liver and muscle. In obesity, hypoxia within adipose tissue can induce inflammation and there is a reported association between GIP and hypoxic signalling in adipose tissue inflammation. GIP receptor antagonism has been observed to reverse obesity, insulin resistance, and associated metabolic disturbances in mice.
Obesity is perceived to be the most significant health issue in companion animal nutrition with reports indicating that as many as 35-40% of cats and dogs are overweight/obese (Lund et. al., 2005; German, 2006). The accumulation of excess body fat has many detrimental effects on the health of animals including impaired glucose tolerance (insulin resistance), type 2 diabetes and chronic low grade tissue inflammation. Multiple factors are likely to be involved in weight gain and the development of obesity in cats and dogs, some of which may be considered to be intrinsic to the animal (e.g. genes, level of spontaneous physical activity), whilst others may be extrinsic (e.g. the amount and frequency of food provision). In companion animals, where food provision is almost exclusively determined by the carer/owner, it might be thought that the amount of food provided could be easily controlled to avoid weight gain. However, variability in the measuring of food portions has been shown to range from an 18% under-estimate to an 80% over-estimate in portion size, which over time could markedly affect body weight (German et. al., 2011).
Pet obesity is a major concern for companion animal health and nutrition. There is a need to control the body fat in companion animals. Many animal owners unintentionally over feed their animals. Companion animals do not control the amount of food they eat as their instinct is to eat as much as possible when food is available. For that reason, domestic animals tend to gain weight.
There is therefore a need to provide pet food products which aids companion animals to avoid the accumulation of body fat and therefore help to maintain a “healthy” body composition and controlling body weight of the companion animal, which will help to reduce the risk and/or prevent the development of health problems, such as insulin resistance and type 2 diabetes.